Serial Diffusion Tensor Imaging of the Optic Radiations after Acute Optic Neuritis.

Scott C Kolbe,Trevor J Kilpatrick,Gary F Egan,Anneke Van Der Walt,Helmut Butzkueven,Alexander Klistorner

doi:10.1155/2016/2764538

Abstract

Previous studies have reported diffusion tensor imaging (DTI) changes within the optic radiations of patients after optic neuritis (ON). We aimed to study optic radiation DTI changes over 12 months following acute ON and to study correlations between DTI parameters and damage to the optic nerve and primary visual cortex (V1). We measured DTI parameters [fractional anisotropy (FA), axial diffusivity (AD), radial diffusivity (RD), and mean diffusivity (MD)] from the optic radiations of 38 acute ON patients at presentation and 6 and 12 months after acute ON. In addition, we measured retinal nerve fibre layer thickness, visual evoked potential amplitude, optic radiation lesion load, and V1 thickness. At baseline, FA was reduced and RD and MD were increased compared to control. Over 12 months, FA reduced in patients at an average rate of −2.6% per annum (control = −0.51%; p = 0.006). Change in FA, RD, and MD correlated with V1 thinning over 12 months (FA: R = 0.450, p = 0.006; RD: R = −0.428, p = 0.009; MD: R = −0.365, p = 0.029). In patients with no optic radiation lesions, AD significantly correlated with RNFL thinning at 12 months (R = 0.489, p = 0.039). In conclusion, DTI can detect optic radiation changes over 12 months following acute ON that correlate with optic nerve and V1 damage.

Highlights

In later stages of multiple sclerosis (MS), patients can develop a “secondary progressive” (SPMS) disease phenotype that is not associated with neuroinflammatory relapses but rather with axonal injury and primary neuronal pathologies
No other diffusion tensor imaging (DTI) parameters displayed a significant longitudinal change; there was a trend towards a significant increase in radial diffusivity (RD) in patients (2.82 ± 0.61%) compared to controls (1.30 ± 0.48%, p = 0.06)
Longitudinal change in fractional anisotropy (FA), RD, and mean diffusivity (MD) significantly correlated with V1 thinning

Summary

Introduction

In later stages of multiple sclerosis (MS), patients can develop a “secondary progressive” (SPMS) disease phenotype that is not associated with neuroinflammatory relapses but rather with axonal injury and primary neuronal pathologies. To develop new treatments for secondary progressive MS, it is critical to identify the disease mechanisms underlying the transition from relapsing-remitting to SPMS. Several candidate neurodegenerative processes have been proposed, including excitotoxicity and transsynaptic degeneration [1]. Transsynaptic degeneration occurs when a neuron loses afferent input or efferent targets. The precise molecular mechanisms of transsynaptic degeneration continue to be investigated. Given that multifocal sites of neuroinflammatory injury in MS can transect axons throughout the central nervous system, transsynaptic degenerative processes could be responsible for nonlesional, secondary neurodegeneration in neural circuits in the brain

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